This invention is in the field of transformed plants, particularly potatoes, which have been rendered resistant to disease, including the very destructive disease known as late blight, caused by Phytophthora infestans. 
One of the agronomically most important diseases is caused by the fungal pathogen P. infestans. In potato it causes late blight disease. Late blight epidemics have caused a persistent threat to potato growers since the Irish Famine in the early 1800s, and late blight has re-emerged as a devastating disease in the United States with the recent establishment of a new clonal lineage of P. infestans, designated A2 isolate US-8. During the mid 1990s, this unusually aggressive lineage replaced an earlier predominant lineage within only two years, and has caused severe epidemics since then, resulting in annual potato losses exceeding 100 million dollars. There are currently no cost-effective means of US-8 control because none of the commercially-available cultivars in the United States contain disease resistance (R-) genes against this pathogen, which is also resistant to the fungicide metalaxyl.
The lack of effective R-genes in cultivated potato is due, in part, to the absence of R-gene breeding programs. Such efforts were discouraged by the fact that eleven R-genes from the resistant wild potato species Solanum demissum that had been introgressed into potato in the 1960s resulted in temporary control of late blight only (Landeo et al., In: Phytophthora infestans. Ed. Dowley L J et al., Bole Press Ltd. Dublin, Ireland, 268–274, 1995). Apparently, the agricultural use of R-genes for late blight control results in the establishment of races that are not recognized by R-genes, through rapid shifts in population dynamics of P. infestans. 
An important biotechnology strategy to enhance disease resistance in plants is based on the identification and expression of antifungal proteins (AFP's). Reported AFP classes include defensins and other small cysteine-rich peptides, 2S albumins, chitin-binding proteins, lipid transfer proteins, and hydrogen peroxide-generating enzymes (Garcia-Olmedo et al., Biopolymers 47: 479–491, 1998). Unfortunately, the constitutive overexpression of AFP's in transgenic plants has not yet resulted in commercially relevant levels of late blight disease control. Thus, none of the conventional breeding and biotechnology approaches have resulted in the generation of potato cultivars displaying durable late blight resistance.
It is well established that the enzyme polyphenol oxidase (PPO) is the enzyme which catalyzes the conversion of phenolic substrates, predominantly tyrosine, to melanin in many plant species. PPO is the major cause of enzymatic browning in higher plant tissues, including that of potato. Polyphenol oxidases are plastid membrane-associated, copper metalloproteins which catalyze the hydroxylation of monophenols to o-diphenols, and the dehydrogenation of o-diphenols to o-diquinones in the presence of oxygen. The quinone products undergo a series of nonenzymatic secondary autooxidation reactions to produce highly reactive electrophiles which form melanin, as well as covalently crosslink with amine groups of cellular proteins, resulting in brown and black pigment production (Newman, et al., Plant Mol. Biol. 21:1035–1051, 1993; Thygesen, et al., Plant Physiol. 109:525–531, 1995). PPO is also present in non-photosynthetic tissues, and in potato tubers PPO is associated with amyloplasts of tuber cells. In potato tubers, the primary phenolic substrate for PPO is tyrosine, which exists at high levels in the free amino acid pool. PPO utilizes organic acids such as chlorogenic acid and caffeic acid much more rapidly than tyrosine, but these substrates exist in potato tubers at significantly lower levels than tyrosine and are therefore not the primary substrates for PPO in the tuber. PPO catalyzes the slow conversion of tyrosine to dihydroxyphenyl-alanine (DOPA), and rapid conversion of DOPA to DOPA quinone, which autooxidizes to form brown and black melanin pigmentation. Enzymatic browning mediated by PPO occurs when tuber tissue is damaged, usually by physical impact or long-term pressure, and loss of intracellular compartmentalization results, thereby allowing PPO to come into contact with tyrosine. In damaged tissue regions with dark melanin formation, commonly referred to as black spot bruises, the cell walls do not need to be broken, only disruption of intracellular membrane integrity is required (Craft, Am. Pot. J. 43: 112–121, 1966; Stark et al., Am. Pot. J. 62: 657–666, 1985; Corsini et al., Am. Pot. J. 69: 423–434, 1992).
In potato tubers, it is the action of the PPO enzyme which leads to the formation of black spot bruises after physical impact or damage to tuber tissue. It is theorized that the reduced expression of PPO, through transformation with a DNA construct in antisense orientation or through transformation and cosuppression, use of a double-stranded mRNA (dsRNA) construct, the simultaneous expression of both sense and antisense RNA, or other effective means of reduced expression of PPO in potatoes will result in reduced susceptibility of tubers to exhibit black spot bruises (see PCT Patent Applications WO 93/02195, 93/15599, and 94/03607).
It has been previously thought that PPO played a role in the plant's innate resistance to disease and therefore that reduced expression of PPO would render the plant more susceptible to disease (see for example WO 93/15599, page 4). However, it has surprisingly been discovered in the present invention that the opposite result is possible, that is, reduced expression of PPO can render a plant more resistant to disease.